The length of the renal papilla determines urinary concentrating capacity. Angiotensin II (A II) may play a role in development and maintenance of the papilla, as suggested by the papillary atresia found in knockout mice lacking A II. the pathogenesis of this papillary atresia is not understood. It has not been reproduced by disruption of either AT1A [Agtr1A] or AT2 A II receptor genes on mixed genetic backgrounds, although Agtr1A (-/-) mice have a concentrating defect. AT1A deficient mice with a >97% C57 BL/6 genetic background [B6Agtr1A (-/)] have a concentrating defect at 4 months of age, and develop papillary atresia by 8 months. Exclusion of subtle papillary abnormalities in Agtr1A (-/-) mice, and examination of the time course of the papillary changes to B6Agtr1A (-/-) has been difficult using standard methods. We propose to use MRM to better visualize the renal papillary in these mouse models